Nakamura Katrina, Sheps Sam, Arck Petra Clara
Interdisciplinary Studies Graduate Program, University of British Columbia, 6201 Cecil Green Park Road, Vancouver, BC, V6T 1Z1, Canada.
J Assist Reprod Genet. 2008 Feb-Mar;25(2-3):47-62. doi: 10.1007/s10815-008-9206-5. Epub 2008 Feb 15.
Maternal stress perception is frequently alleged as a cause of infertility, miscarriages, late pregnancy complications or impaired fetal development. The purpose of the present review is to critically assess the biological and epidemiological evidence that considers the plausibility of a stress link to human reproductive failure.
All epidemiological studies published between 1980 and 2007 that tested the link between stress exposure and impaired reproductive success in humans were identified. Study outcomes were evaluated on the basis of how associations were predicted, tested and integrated with theories of etiology arising from recent scientific developments in the basic sciences. Further, published evidence arising from basic science research has been assessed in order to provide a mechanistic concept and biological evidence for the link between stress perception and reproductive success.
Biological evidence points to an immune-endocrine disequilibrium in response to stress and describes a hierarchy of biological mediators involved in a stress trigger to reproductive failure. Epidemiological evidence presents positive correlations between various pregnancy failure outcomes with pre-conception negative life events and elevated daily urinary cortisol. Strikingly, a relatively new conceptual approach integrating the two strands of evidence suggests the programming of stress susceptibility in mother and fetus via a so-called pregnancy stress syndrome.
An increasing specificity of knowledge is available about the types and impact of biological and social pathways involved in maternal stress responses. The present evidence is sufficient to warrant a reconsideration of conventional views on the etiology of reproductive failure. Physicians and patients will benefit from the adaptation of this integrated evidence to daily clinical practice.
孕产妇的压力感知常被认为是导致不孕、流产、晚期妊娠并发症或胎儿发育受损的原因。本综述的目的是严格评估生物学和流行病学证据，以考量压力与人类生殖失败之间存在关联的合理性。
检索了1980年至2007年间发表的所有测试压力暴露与人类生殖成功率受损之间关联的流行病学研究。根据关联的预测、测试方式以及与基础科学最新科学发展所产生的病因学理论的整合情况来评估研究结果。此外，还评估了基础科学研究已发表的证据，以便为压力感知与生殖成功之间的联系提供一个机制概念和生物学证据。
生物学证据表明，应激反应会导致免疫 - 内分泌失衡，并描述了一系列参与应激引发生殖失败的生物介质。流行病学证据显示，各种妊娠失败结果与孕前负面生活事件以及每日尿皮质醇升高之间存在正相关。引人注目的是，一种整合这两类证据的相对较新的概念方法表明，通过一种所谓的妊娠应激综合征，母亲和胎儿的应激易感性会被编程。
关于孕产妇应激反应所涉及的生物学和社会途径的类型及影响，人们掌握的知识越来越具体。目前的证据足以促使人们重新审视关于生殖失败病因的传统观点。医生和患者将从将这一整合证据应用于日常临床实践中受益。
